Possible retroviral origin of prion diseases.
The proposed hypothesis that a retrovirus might be involved in the etiology of spongiform encephalopathies, integrates experimental results obtained from different fields of research. While retroviral genes themselves may be responsible for neuronal death, a retrovirus may also cause mutations in cellular genes. Hence, the prion gene may be altered by a retrovirus in the same way as a cellular proto-oncogene is altered to give an oncogene, either by transduction or by integration of the provirus in its vicinity. In both cases, the resulting abnormal prion protein, acting as a catalyst, may induce the formation of amyloid plaques. In addition, a wild type retrovirus may recombine to the vesicular stomatitis virus (VSV) to give rise to a pseudotyped retrovirus carrying the VSV G gene, known to induce spongiosis. Therefore a retroviral etiology might explain why amyloid plaque and/or spongiosis are or are not associated with neuronal death in prion diseases.
Labat
M L
ML
Laboratoire de Physiopathologie Osseuse, Institut Biomédical des Cordeliers, Paris, France.
D000818:Animals; D005814:Genes, Viral; D006801:Humans; D008954:Models, Biological; D009474:Neurons / Q000473:pathology / Q000502:physiology; D017096:Prion Diseases / Q000821:virology*; D000090063:Proto-Oncogene Mas; D012190:Retroviridae / Q000472:pathogenicity*; D014721:Vesicular stomatitis Indiana virus / Q000472:pathogenicity